The goal is to elucidate the biological basis for the very consistent and well-documented epidemiological observation that there is an inverse relationship between cigarette smoking and PD. Cigarette smoke contains numerous chemicals which could conceivably be neuroprotective. However, most research to date has focused on nicotine because of its well-known ability to, (1) stimulate striatal dopamine release and (2) exert a neuroprotective effect both in vitro and in vivo. In most studies, including this one, this neuroprotection is significant but relatively modest (approximately 20%) in the rodent model. Nicotine mediates its effects through an interaction with nicotinic receptors, of which there are multiple subtypes. The investigators have found that alpha-6*nicotinic receptors (*denotes receptors containing the indicated subunit) appear to be preferentially localized to dopaminergic neurons, and are selectively vulnerable to nigrostriatal damage. Importantly, the investigators? results also indicate that monkeys have a greater proportion of striatal alpha-6*nicotinic receptors than mice (50% versus 15%respectively). Based on these findings, the investigators hypothesize (1) that alpha-6* receptors play a key role in nicotine-induced neuroprotection, and (2) that this effect will be more pronounced in monkeys as compared to rodents. They will also explore a potential mechanism by which this effect occurs by assessing nicotine-induced changes in neurotrophic factors.